• Expression of VEGF, E2F8, COL6A1, IGFBP2, PLK1, RB1, RBL1 and TP53 genes in pediatric glioma
To content

Expression of VEGF, E2F8, COL6A1, IGFBP2, PLK1, RB1, RBL1 and TP53 genes in pediatric glioma

SOVREMENNAYA PEDIATRIYA. 2015.1(65):126-129; doi 10.15574/SP.2015.65.126

 

Expression of VEGF, E2F8, COL6A1, IGFBP2, PLK1, RB1, RBL1 and TP53 genes in pediatric glioma

 

Minchenko D. O.

Department of Pediatrics №1, National O.O. Bohomolets Medical University, Kyiv, Ukraine;

Department of Molecular Biology, Palladin Institute of Biochemistry National Academy of Sciences of Ukraine, Kyiv, Ukraine;

 

Objective. The goal of this study was to study in pediatric glioma the peculiarity of the expression of genes related to dysregulation of proliferation processes in malignant tumors.

 

Materials and Methods. The glioma tissue from 4 children with age from 5 to 8 years as well as corresponding non-malignant tissue counterparts were used in this study. RNA was isolated from glioma tissue and corresponding non-malignant tissue counterparts (control) and VEGF, E2F8, COL6A1, IGFBP2, PLK1, RB1, RBL1, and TP53 gene expressions were studied by quantitative polymerase chain reaction.

 

Results. It was shown that the expression level of VEGF, E2F8, COL6A1, IGFBP2, and PLK genes is increased, but RB1, RBL1, and TP-3 genes significantly decreased as compared to corresponding non-malignant tissue counterparts. More significant changes were demonstrated for COL6A1, VEGF, and IGFBP2 genes, which encoded the important regulatory proteins of extracellular matrix.

 

Conclusions. The obesity affects the expression of the subset of genes related to the control of glycolysis in blood cells, but insulin resistance in obesity is associated only with changes in the expression level of ENO1 and ENO2 genes, which possibly contribute to the development of insulin resistance as well as glucose intolerance.

 

Key words: glioma, children, gene expression, VEGF, E2F8, COL6A1, IGFBP2, PLK1, TP-3.

 

REFERENCES

1. De Bonis P, Marziali G, Vigo V et al. 2013. Anti_angiogenic treatment for high-grade gliomas: current concepts and limitations. Expert Rev Neurother. 13;11: 1263—1270.

2. Bakker WJ, Weijts BG, Westendorp B, de Bruin A. 2013. HIF proteins connect the RB-E2F factors to angiogenesis. Transcription. 4;2: 62—66.

3. Chang YC, Wu CH, Yen TC, Ouyang P. 2012. Centrosomal protein 55 (Cep55) stability is negatively regulated by p53 protein through Polo-like kinase 1 (Plk1). J Biol Chem. 287;6: 4376—4385.

4. Comstock CE, Augello MA, Schiewer MJ et al. 2011. Cyclin D1 is a selective modifier of androgen-dependent signaling and androgen receptor function. J Biol Chem. 286;10: 8117—8127.

5. Diaz AK, Baker SJ. 2014. The genetic signatures of pediatric high_grade glioma: no longer a one-act play. Semin Radiat Oncol. 24;4: 240—247.

6. Deng Q, Wang Q, Zong WY et al. 2010. E2F8 contributes to human hepatocellular carcinoma via regulating cell proliferation. Cancer Res. 70;2: 782—791.

7. Ewald JA, Downs TM, Cetnar JP, Ricke WA. 2013. Expression microarray meta-analysis identifies genes associated with Ras/MAPK and related pathways in progression of muscle-invasive bladder transition cell carcinoma. PLoS One. 8;2: e55414.

8. Golubovskaya VM, Cance WG. 2013. Targeting the p53 pathway. Surg Oncol Clin N Am. 22;4: 747—764.

9. Hsieh А, Stea B, Ellsworth R. 2010. IGFBP2 promotes glioma tumor stem cell expansion and survival. Biochem Biophys Res Commun. 397;2: 367—372.

10. Fujita A, Sato JR, Festa F et al. 2008. Identification of COL6A1 as a differentially expressed gene in human astrocytomas. Genet Mol Res. 7;2: 371—378.

11. Kachaner D, Filipe J, Laplantine E. 2012. Plk1-dependent phosphorylation of optineurin provides a negative feedback mechanism for mitotic progression. Mol Cell. 45;4: 553—566.

12. Bhola NE, Jansen VM, Bafna S et al. 2015. Kinome-wide Functional Screen Identifies Role of PLK1 in Hormone-In-dependent, ER-Positive Breast Cancer. Cancer Res. 75;2: 405—414.

13. Mills KD. 2013. Tumor suppression: putting p53 in context. Cell Cycle. 12;22: 3461—3462.

14. Bochkov VN, Philippova M, Oskolkova O et al. 2006. Oxidized phospholipids stimulate angiogenesis via induction of VEGF, IL-8, COX-2 and ADAMTS-1 metalloprotease, implicating a novel role for lipid oxidation in progression and destabilization of athe- rosclerotic lesions. Circ Res. 99;8: 900—908.

15. Zhou Z, Cao JX, Li SY et al. 2013. P53 Suppresses E2F1_dependent PLK1 expression upon DNA damage by forming p53-E2F1-DNA complex. Exp Cell Res. 319;20: 3104—3115.

16. Thalhammer V, Lopez-Garcia LA, Herrero-Martin D et al. 2015. PLK1 phosphorylates PAX3-FOXO1, the inhibition of which triggers regression of alveolar rhabdomyosarcoma. Cancer Res. 75;1: 98—110.